Molecular basis of bacterial outer membrane permeability.

Protein phosphorylation and regulation of adaptive responses in bacteria.

A colony bank containing synthetic CoI EI hybrid plasmids representative of the entire E. coli genome

Proton-dependent multidrug efflux systems.

We provide the first evidence that the size (diameter) of carbon nanotubes (CNTs) is a key factor governing their antibacterial effects and that the likely main CNT-cytotoxicity mechanism is cell membrane damage by direct contact with CNTs. Experiments with well-characterized single-walled carbon nanotubes (SWNTs) and multiwalled carbon nanotubes (MWNTs) demonstrate that SWNTs are much more toxic to bacteria than MWNTs. Gene expression data show that in the presence of both MWNTs and SWNTs, Escherichia coli expresses high levels of stress-related gene products, with the quantity and magnitude of expression being much higher in the presence of SWNTs.

Antibacterial Effects of Carbon Nanotubes: Size Does Matter!

By using each of the available colicins, we have isolated a large number of colicin-resistant mutants. They included both receptor and tolerant mutants and each was screened for cross-resistance to all other colicins. On the basis of the cross-resistance of these mutants it was possible to place known colicins into two mutually exclusive groups, group A and group B. Mutants selected as resistant to colicins of group A may or may not be cross-resistant to other colicins of group A, BUT Are never resistant to colicins of group B. The reverse also applies. The mutants isolated as resistant to colicins of group A (A, E1, E2, E3, K, L, N, S4, and X) have been divided into 21 phenotypic classes on the basis of their colicin resistance patterns. These include most of the tolerant and receptor mutants previously isolated, some of which were previously shown to also have an increased sensitivity to certain antibiotics and detergents. Type strains from each of the phenotypic classes were therefore tested for sensitivity to a range of antibiotics, detergents, and surfactants that included all those previously used. With these new data, it has been possible to speculate informatively on the mode of action of the different colicins. We have confirmed the position of previously isolated mutations on the Escherichia coli K-12 genetic map, and located approximately the loci conferring colicin resistance in some of the newly isolated mutants.

Genetics of resistance to colicins in Escherichia coli K-12: cross-resistance among colicins of group A.

Cross-resistance between bacteriophages and colicins was studied using collections of bacteriophage- and colicin-resistant mutants of Escherichia coli K-12. No new examples were found of highly specific one-to-one cross-resistance of the type suggestive of common receptors. However, several groups of mutants showed tolerance to colicins and resistance to bacteriophages. Mutants known to be very defective in lipopolysaccharides composition were found to commonly show tolerance to certain colicins in addition to their bacteriophage resistance. Another group of mutants showed varying patterns of resistance to colicins E2, E3, K, L, A, S4, N, and X and bacteriophages E4, K2, K20, K21, K29, and H+. However, many bacteriophage-resistant mutants were fully colicin sensitive, and most colicin-resistant mutants were fully sensitive to bacteriophages.

Cross-resistance between bacteriophages and colicins in Escherichia coli K-12.

Con minus mutants, conjugation-defective mutants of Escherichia coli K-12, have been shown to be tolerant to colicins K and L. They map at approximately 14 min on the genetic map. The significance of the colicin tolerance of conjugation-defective mutants is discussed.

J K Davies

Papers

Genetics of resistance to colicins in Escherichia coli K-12: cross-resistance among colicins of group A.

Cross-resistance between bacteriophages and colicins in Escherichia coli K-12.

Colicin tolerance and map location of conjugation-deficient mutants.